Evidence map›Paper›PMID 18198337›Full record

ArticleGenes & development2008

Meiotic crossover number and distribution are regulated by a dosage compensation protein that resembles a condensin subunit.

Chun J Tsai, David G Mets, Michael R Albrecht, Paola Nix, Annette Chan, Barbara J Meyer

Abstract read
In one paragraph

Article in Genes & development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

75 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The X chromosome in C. elegans sex determination and dosage compensation.Current opinion in genetics & development · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Meiosis.WormBook : the online review of C. elegans biology · 2017
    Review
  17. Article
  18. Review
  19. Article
  20. Article

15 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Chun J TsaiHoward Hughes Medical Institute, Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, CA 97420, USA.
David G Mets
Michael R Albrecht
Paola Nix
Annette Chan
Barbara J Meyer

Funding

THE MOLECULAR BASIS OF CELL FUNCTIONT32GM007232 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI BILDER, DAVID, UNAL, ELCIN · 1985 to 2022
$36.4M
POSTGRADUATE TRAINING PROGRAM IN GENETICST32GM007127 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI DILLIN, ANDREW G · 1985 to 2016
$7.9M
NEMATODE SEX DETERMINATIONR01GM030702 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MEYER, BARBARA J · 1985 to 2018
$6.1M
NIGMS NIH HHS R01 GM030702NIGMS NIH HHS R01 GM 30702NIGMS NIH HHS T32 GM007127NIGMS NIH HHS T32 GM 007232NIGMS NIH HHS T32 GM007232NIGMS NIH HHS T32 GM 07127
6 · The paper itself

Abstract

Biological processes that function chromosome-wide are not well understood. Here, we show that the Caenorhabditis elegans protein DPY-28 controls two such processes, X-chromosome dosage compensation in somatic cells and meiotic crossover number and distribution in germ cells. DPY-28 resembles a subunit of condensin, a conserved complex required for chromosome compaction and segregation. In the soma, DPY-28 associates with the dosage compensation complex on hermaphrodite X chromosomes to repress transcript levels. In the germline, DPY-28 restricts crossovers. In many organisms, one crossover decreases the likelihood of another crossover nearby, an enigmatic process called crossover interference. In C. elegans, interference is complete: Only one crossover occurs per homolog pair. dpy-28 mutations increase crossovers, disrupt crossover interference, and alter crossover distribution. Early recombination intermediates (RAD-51 foci) increase concomitantly, suggesting that DPY-28 acts to limit double-strand breaks (DSBs). Reinforcing this view, dpy-28 mutations partially restore DSBs in mutants lacking HIM-17, a chromatin-associated protein required for DSB formation. Our work further links dosage compensation to condensin and establishes a new role for condensin components in regulating crossover number and distribution. We propose that both processes utilize a related mechanism involving changes in higher-order chromosome structure to achieve chromosome-wide effects.

Indexed as

Dosage Compensation, GeneticMeiosisX ChromosomeAdenosine TriphosphatasesAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell Cycle ProteinsChromosome BreakageCrossing Over, GeneticDisorders of Sex DevelopmentDNA-Binding ProteinsEpigenesis, GeneticMultiprotein ComplexesMutationAdenosine TriphosphatasesCaenorhabditis elegans ProteinsCell Cycle Proteinscondensin complexesDNA-Binding ProteinsHIM-17 protein, C elegansMultiprotein ComplexesSdc-3 protein, C elegans

Identifiers

PMID18198337
PMCPMC2192754

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.